Let‐7 as biomarker, prognostic indicator, and therapy for precision medicine in cancer.

publisher‐imprint‐name Springer volume‐issue‐count 1 issue‐article‐count 0 issue‐toc‐levels 0 issue‐pricelist‐year 2019 issue‐copyright‐holder The Author(s) issue‐copyright‐year 2019 article‐contains‐esm No article‐numbering‐style Unnumbered article‐registration‐date‐year 2019 article‐registration‐date‐month 8 article‐registration‐date‐day 16 article‐toc‐levels 0 toc‐levels 0 volume‐type Regular journal‐product ArchiveJournal numbering‐style Unnumbered article‐grants‐type OpenChoice metadata‐grant OpenAccess abstract‐grant OpenAccess bodypdf‐grant OpenAccess bodyhtml‐grant OpenAccess bibliography‐grant OpenAccess esm‐grant OpenAccess online‐first false pdf‐file‐reference BodyRef/PDF/40169_2019_Article_240.pdf target‐type OnlinePDF issue‐type Regular article‐type ReviewPaper journal‐subject‐primary Medicine & Public Health journal‐subject‐secondary Medicine/Public Health, general journal‐subject‐collection Medicine open‐access true --> Abnormal regulation and expression of microRNAs (miRNAs) has been documented in various diseases including cancer. The miRNA let‐7 (MIRLET7) family controls developmental timing and differentiation. Let‐7 loss contributes to carcinogenesis via an increase in its target oncogenes and stemness factors. Let‐7 targets include genes regulating the cell cycle, cell signaling, and maintenance of differentiation. It is categorized as a tumor suppressor because it reduces cancer aggressiveness, chemoresistance, and radioresistance. However, in rare situations let‐7 acts as an oncogene, increasing cancer migration, invasion, chemoresistance, and expression of genes associated with progression and metastasis. Here, we review let‐7 function as tumor suppressor and oncogene, considering let‐7 as a potential diagnostic and prognostic marker, and a therapeutic target for cancer treatment. We explain the complex regulation and function of different let‐7 family members, pointing to abnormal processes involved in carcinogenesis. Let‐7 is a promising option to complement conventional cancer therapy, but requires a tumor specific delivery method to avoid toxicity. While let‐7 therapy is not yet established, we make the case that assessing its tumor presence is crucial when choosing therapy. Clinical data demonstrate that let‐7 can be used as a biomarker for rational precision medicine decisions, resulting in improved patient survival. [ABSTRACT FROM AUTHOR]